GKLF as a Novel Target in Selenium Chemoprevention of Prostate Cancer

2008 ◽  
Author(s):  
Yan Dong
Keyword(s):  
Prostate Cancer ◽  
Novel Target

Cannabinoid Receptors: A Novel Target for Treating Prostate Cancer

2006 ◽  
Author(s):  
Hasan Mukhtar ◽  
Farrukh Afaq ◽  
Sami Sarfaraz
Keyword(s):  
Prostate Cancer ◽  
Cannabinoid Receptors ◽  
Novel Target

scholarly journals LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Enhui Ma ◽  
Qianqian Wang ◽  
Jinhua Li ◽  
Xinqi Zhang ◽  
Zhenjia Guo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prostate Gland ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Protein Coding ◽  
Novel Target

Abstract Background Prostate cancer (PCa) is a kind of malignancy occurring in the prostate gland. Substantial researches have proved the major role of long noncoding RNAs (lncRNAs) in PCa. However, the role of long intergenic non-protein coding RNA 1006 (LINC01006) in PCa has not been investigated yet. Methods RT-qPCR was used to examine the expression levels of LINC01006 and its downstream targets. The function of LINC01006 in PCa was tested by in vitro and in vivo assays. With application of RNA pull down, RNA immunoprecipitation (RIP) and luciferase reporter assays, the interaction among LINC01006, miR-34a-5p and disheveled associated activator of morphogenesis 1 (DAAM1) were verified. Results LINC01006 expression presented high in PCa cell lines. LINC01006 silencing suppressed cell proliferative, migratory, invasive capacities while accelerated apoptotic rate. Besides, LINC01006 knockdown also suppressed tumor growth and metastasis in vivo. Furthermore, miR-34a-5p, a tumor suppressor in PCa, was sponged by LINC01006. Moreover, DAAM1 was targeted by miR-34a-5p and promoted PCa progression. More intriguingly, rescue assays suggested that the inhibitory effect of LINC01006 knockdown on PCa development was offset by DAAM1 overexpression. Conclusions LINC01006 promoted PCa progression by sponging miR-34a-5p to up-regulate DAAM1, providing a novel target for PCa therapy.

scholarly journals MCT4 is a novel target for prostate cancer

2016 ◽  
Vol 13 (3) ◽  
pp. 123-123
Author(s):  
Rebecca Kelsey
Keyword(s):  
Prostate Cancer ◽  
Novel Target

scholarly journals 1002. L1 Cell Adhesion Molecule, a Novel Target of Prostate Cancer Gene Therapy

2006 ◽  
Vol 13 ◽  
pp. S386
Author(s):  
Kristen Bisanz ◽  
Jie Yu ◽  
Ira Rajbhandari ◽  
Bill Spohn ◽  
Mien-Chie Hung ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Gene Therapy ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Cancer Gene Therapy ◽  
Cancer Gene ◽  
Novel Target ◽  
L1 Cell Adhesion Molecule

scholarly journals CXCR4 Is a Novel Target of Cancer Chemopreventative Isothiocyanates in Prostate Cancer Cells

2015 ◽  
Vol 8 (5) ◽  
pp. 365-374 ◽  
Author(s):  
Kozue Sakao ◽  
Avani R. Vyas ◽  
Sreenivasa R. Chinni ◽  
Ali I. Amjad ◽  
Rahul Parikh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Novel Target

scholarly journals Extracellular Microenvironment in Patient-derived Hydrogel Organoids of Prostate Cancer Regulates Therapeutic Response

2020 ◽  
Author(s):  
Matthew J Mosquera ◽  
Rohan Bareja ◽  
Jacob M Bernheim ◽  
Muhammad Asad ◽  
Cynthia Cheung ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Inflammatory Cells ◽  
Cellular Reprogramming ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant ◽  
Prostate Cells ◽  
Synthetic Hydrogel ◽  
Neuroendocrine Prostate Cancer ◽  
Prostate Cancers ◽  
Novel Target

Following treatment with androgen receptor (AR) pathway inhibitors, ~20% of prostate cancer patients progress by shedding their dependence on AR. These tumors undergo epigenetic reprogramming turning castration-resistant prostate cancer adenocarcinoma (CRPC-Adeno) into neuroendocrine prostate cancer (CRPC-NEPC). Currently, no targeted therapies are available for CRPC-NEPCs. A major hurdle in the development of new therapies and treatment of CRPC-NEPC is the lack of accurate models to test candidate treatments. Such models would ideally capture components of the tumor microenvironment (TME) factors, which likely regulate the phenotypic, genetic, and epigenetic underpinnings of this aggressive subset. The TME is a complex system comprised not only of malignant prostate cells but also stromal and inflammatory cells and a scaffold of extracellular matrix (ECM). ECM proteins are implicated in the survival and progression of cancer and development of chemoresistance, while are equally integral to the development of prostate cancer organoids. Here, using a combination of patient tumor proteomics and RNA sequencing, we define putative ECM cues that may guide the growth of prostate tumors in patients. Using this molecular information, we developed synthetic hydrogels that recapitulate the tumor ECM. Organoids cultured in the synthetic hydrogel niches demonstrate that ECM subtypes regulate the morphology, transcriptome, and epigenetics hallmarks of CRPC-Adeno and CRPC-NEPC. CRPC-NEPC organoid showed a differential response to small molecule inhibitors of epigenetic repressor EZH2 and Dopamine Receptor D2 (DRD2), the latter being a novel target in CRPC-NEPC when grown in tumor-specific ECM. Finally, in those synthetic ECM niches where drug resistance was observed in CRPC-NEPCs, cellular reprogramming by a synergistic combination of EZH2 inhibitors with DRD2 antagonists inhibited tumor growth. The synthetic platform can provide a more realistic prostate-specific microenvironment and subsequently enable the development of effective targeted therapeutics for prostate cancers.

scholarly journals The BIRC6 gene as a novel target for therapy of prostate cancer: dual targeting of inhibitors of apoptosis

Oncotarget ◽  
2014 ◽  
Vol 5 (16) ◽  
pp. 6896-6908 ◽  
Author(s):  
Sze Ue Iris Luk ◽  
Hui Xue ◽  
Hongwei Cheng ◽  
Dong Lin ◽  
Peter W. Gout ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Inhibitors Of Apoptosis ◽  
Dual Targeting ◽  
Novel Target
Sign in / Sign up

Export Citation Format

Share Document